Chronic obstructive pulmonary disease (COPD), consisting of emphysema and chronic bronchitis, is the fourth leading cause of death in the United States(1). Approximately 15 million Americans are affected by COPD and there is an increasing incidence in women(2). Smoking is the major risk factor for COPD and accounts for over 90% of cases seen worldwide. Despite the importance of the disease, there are no specific therapies available to limit or prevent the slow, progressive, destructive changes observed in COPD(3).
Currently the major hypothesis for the pathogenesis of emphysema is the protease-antiprotease theory(4,5). This model suggests that an imbalance between the levels of extracellular matrix degrading enzymes and their respective inhibitors damage the connective tissue matrix components. of the lung. Studies over the past 30 years have demonstrated differences in the protease levels in the lung of patients with emphysema when compared to normal lung tissue(6). However, the molecular consequences of this finding have not been determined.
Although studies have demonstrated loss of the extracellular matrix in the lung of patients with emphysema, an investigation as to whether cell death contributes to the pathogenesis of this disease has not been performed.